Primary biliary cirrhosis (PBC) is chronic liver disease of unknown etiology. Histologically, PBC is characterized by a progressive immunologically mediated inflammation known as chronic nonsuppurative destructive cholangitis (CNSDC) that leads to bile duct destruction, ductopenia and biliary cirrhosis. At present there is no cure for PBC. The most common symptoms associated with PBC are fatigue and pruritus. More than 90% of patients with PBC are women. The average age of diagnosis is about 50 years. Asymptomatic patients have a four-fold increase in mortality when compared to the U.S.A. population matched for age and the median survival from the onset of symptoms is 7.5 to 9 years. PBC is considered a model autoimmune disease; it is associated with hypergammaglobulinemia, autoantibodies, defects of immune regulation, and an increased incidence of other autoimmune conditions (thyroiditis, Sjogren's syndrome, scleroderma). The liver injury is characterized by a rich inflammatory infiltrate composed of CD4+ and CD8+ cells, cytokines, adhesion molecules and other immunologic mediators. The consequence of CNSDC is biliary cirrhosis and liver failure. The only treatment approved to treat PBC is ursodeoxycholic acid (UDCA), which appears to delay the time to liver transplantation but does not cure for the disease. Thus, the need for the provision of effective and safe treatments for PBC is clear. Patients with PBC may benefit from treatment with an appropriate immunosuppressive drug. Mycophenolate mofetil meets the criteria of a superior immunosuppressive agent. In this proposal we are going to explore immune mediators of PBC including T cells and adhesion molecules in patients with PBC and the effect of treatment with MMF in combination with UDCA on these factors in patients who are participants in a clinical trial.